Riboflavin Deficiency, Brain Function, and Health

Abstract

Vitamin B2 primarily or secondarily participates in a much wider range of critical metabolic pathways than currently recognized. An inherited disorder of the cellular uptake and trafficking of vitamin B2 metabolites may result in poor intestinal absorption, increased urinary loss, and disrupted homeostasis of vitamin B2 metabolites in the CNS. It may affect 10%–15% of the general population and be the most prevalent genetic risk factor for several human diseases. The implications include altered metabolism of several biomolecules and enzyme systems of well-established pathophysiologic relevance such as vitamins B6, B9 (folate), B12, D3, NO, lipids, amino acids, proteins, DNA, cytochrome P-450 and other enzyme systems, HO, and homocysteine. Oxidative stress, and both apoptotic and necrotic phenomena may be enhanced. Due to the loss of the brain privilege for vitamin B2 supply, this inherited condition may be particularly relevant for CNS diseases such as migraine, brain ischemia, traumatic brain injury, neurodegenerative disorders (especially Parkinson and Alzheimer’s diseases), epilepsy, multiple sclerosis, and for Guillain-Barré syndrome, myasthenia, and mitochondrial myopathies. This chapter aims at providing an overview of the potential pathophysiologic, preventive, and therapeutic implications of this prevalent (yet poorly recognized) inherited metabolism disorder for neurological diseases.